171 results about "Caspase 3" patented technology

The present invention relates to methods and compositions for symptom-based differential diagnosis, prognosis, and determination of treatment regimens in subjects. In particular, the invention relates to the use of biomarkers, either individually or in combinations with one another to rule in or out diseases of the aorta and its branches, most particularly aortic aneurysm and/or aortic dissection, and for risk stratification in such conditions. Preferred markers include one or more of creatine kinase-BB (CK-BB), creatine kinase-MB (CK-MB), acidic calponin, basic calponin, B-type natriuretic peptide (BNP), NT-proBNP, proBNP, BNP_79-108, BNP_3-108, caldesmon, caspase-3, D-dimer, soluble elastin fragments, endothelial cell-selective adhesion molecule (ESAM), fibrillin-1, heart-type fatty acid binding protein, MMP-9, myeloperoxidase, myoglobin, smooth muscle myosin, smooth muscle myosin heavy chain, TIMP-1, free cardiac troponin I, complexed cardiac troponin I, free and complexed cardiac troponin I, free cardiac troponin T, complexed cardiac troponin T, and free and complexed cardiac troponin T, and preferred assays are configured to detect these markers.

A unique DHA product, 10, 17S-docosatriene (“Neuroprotectin D1” or “NPD1”), was found to provide surprisingly effective neuroprotection when administered right after an experimental stroke. Moreover, both nerve cells and retinal pigment epithelial (RPE) cells were found to synthesize 10,17S-docosatriene (NPD1) from DHA. NPD1 also potently counteracted H₂O₂/TNFα oxidative stress-mediated cell apoptotic damage. Under the same oxidative-stress conditions, NPD1 up-regulated the anti-apoptotic Bcl-2 proteins, Bcl-2 and Bcl-xL, and decreased expression of the pro-apoptotic proteins, Bad and Bax. Moreover, in RPE cells NPD1 inhibited oxidative stress-induced caspase-3 activation, IL-1β-stimulated human COX-2 promoter expression, and apoptosis due to N-retinylidene-N-retinylethanolamine (A2E). Overall, NPD1 protected both nerve and retinal pigment epithelial cells from cellular apoptosis and damage due to oxidative stress. NPD1 concentration in the brain of Alzheimer's patients was found to be significantly decreased from that of controls. In cultured human brain cells, NPD1 synthesis was up-regulated by neuroprotective soluble β amyloid, and NPD1 was found to inhibit secretion of toxic β amyloid peptides.

Activated protein C (APC), prodrug, and/or a variant thereof may be used as an inhibitor of apoptosis or cell death and/or a cell survival factor, especially for stressed or injured cells or tissues of the nervous system including subjects with neurode-generative disorders. Novel biological functions (e.g., neuroprotection) can be independent or separated from inhibition of clotting or inflammation, and other biological properties of APC (e.g., antithrombotic activity, ability to reduce NFκB-regulated gene expression). It can be used in the treatment of disease or other pathological conditions by at least inhibiting the p53-dependent and/or caspase-3-dependent pro-apoptotic signaling pathways in stressed or injured cells. Thus, APC, prodrugs, and variants thereof (e.g., APC protease domain mutants with reduced anti-coagulant activity) are prototypes of a class of agents for preventing apoptosis or cell death and/or promoting cell survival by direct action on brain cells. New protein C and/or APC variants with reduced anticoagulant activity may be selected thereby.

Inositol hexaphosphate (IP-6) is a polyphosphorylated carbohydrate with potent antioxidant activity to prevent active oxygen species-mediated mutagenesis, cell injury and carcinogenesis. IP-6 also activates DNA repair mechanisms. Sublethal radiation causes DNA damage through the formation of free radicals, reactive oxygen species, and pyrimidine crosslinks leading to cellular proliferation, cell cycle arrest and apoptosis. In the skin it results in the induction of skin cancer, premature skin aging, immuno-suppression, inflammation, and cell death. Likewise sublethal exposure to ionizing radiation as in nuclear blasts (war-time, accidental, terrorist-induced etc), cosmic radiation, etc. also causes the same spectrum of damage to the cells and the organisms with acute symptoms and eventual high risk of many cancers. IP-6 and/or inositol and their pharmaceutically acceptable salts and derivatives, including pyrophosphates and citrate derivatives, significantly counteract the harmful effects of radiation, affecting cell cycle progression in a protective manner (more cells in the protective GI phase) as well as decreasing apoptosis and caspase-3 activation. Various salts of IP-6 are used with comparable efficacy and the combination of IP-6+inositol affords the best protection against radiation-induced cell injury. Thus IP-6 and inositol are effective agents for protection against nuclear, solar and other radiation injuries.

The present invention relates to diagnostic imaging agents for in vivo imaging. The imaging agents comprise a synthetic caspase-3 inhibitor labelled with an imaging moiety suitable for diagnostic imaging in vivo. The invention also provides pharmaceutical and radiopharmaceutical compositions comprising the imaging agents, together with kits for the preparation of the radiopharmaceuticals. Also described are chelator conjugates of the caspase-3 inhibitor, which are suitable for the preparation of imaging agents comprising a radioactive or paramagnetic metal ion. The imaging agents are useful for the diagnostic imaging and or therapy monitoring in vivo of various disease states where caspase-3 is involved.

The invention relates to the use of at least one caspase inhibitor, in particular a caspase-3 inhibitor, for preparing a pharmaceutical composition for the prophylaxis and/or therapy of a viral infection, in particular an infection with an RNA negative-strand virus, preferably an influenza infection, and to a test system for identifying suitable active substances.

The invention provides an acetamide derivative with the structural formula as follows: R represents -X-Ar, -X-COOH, -CO-Ar, -SO2-Ar, -X-Het., or -X-NR1R2, wherein X represents alkylene with 1-8 carbon atoms and the alkylene is not substituted or is substituted by straight chain hydrocarbon or branched hydrocarbon with 1-5 carbon atoms; and Ar represents phenyl, pyridyl, naphthyl, pyrimidyl and quinolyl. The derivative can cause apoptosis by acting on Caspase-3 zymogen in cancer cells and can be widely applied in cancer treatment.

The invention discloses N'-arylmethylene-2-(4-oxothiophene[2,3-d]pyrimidin-3-yl)acetyl hydrazone compounds, and a preparation method and application thereof. The structural general formula of the compounds is shown as a formula (I). Experimental results indicate that the compounds can induce cells to which Caspase-3 in human cervical carcinoma cells, human lung carcinoma cells and human breast carcinoma cells is dependent to die so as to inhibit the propagation of the carcinoma cells, also have low toxicity on normal cells, and can be used for preparing antitumor medicines for treating cervical carcinoma, lung cancer or breast cancer.

Described here are novel, highly selective inhibitors and activity based probes (ABPs) for caspases 3, 7, 8, and 9 and legumain. The compounds selectively inhibit only certain caspases. A positional scanning combinatorial library (PSCL) approach was used to screen pools of peptide acyloxymethyl ketones (AOMKs) containing both natural and non-natural amino acids for activity against a number of purified recombinant caspases. These screens were used to identify structural elements at multiple positions on the peptide scaffold that could be modulated to control inhibitor specificity towards target caspases. Further disclosed are individual optimized covalent inhibitors that could also be equipped with various tags for use as activity based probes, as well as labeled substrates.

The invention discloses application of chlorogenic acid in preparation of medicines for treating cardiomyopathy. The medicines have the effects of up-regulating myocardial specific expression structure genes ACTC1 and corresponding protein, down-regulating caspase-3 genes and corresponding protein thereof, and up-regulating Bc1-2 genes and corresponding protein. The invention also discloses a medicine for treating cardiomyopathy, and the medicine comprises chlorogenic acid and pharmaceutically acceptable auxiliary materials or auxiliary components. The invention also discloses a combined medicine for treating cardiomyopathy.

The invention discloses a caspase 3-sensitive fluorescence enhancement nano developer and a preparation method thereof. The preparation method is characterized by comprising the following steps: obtaining a connection having an appropriate length through simple solid-phase polypeptide synthesis; and obtaining the developer through conventional liquid-phase carboxylic acid/ammonia condensation reaction and fluorescent molecular marker reaction. Under physiologic conditions, the developer has favorable hydrophilicity and is easy to prepare; and meanwhile, the molecule of the fluorescence enhancement nano developer contains an oligopeptide sequence which can be specifically recognized by caspase 3, so that the oligopeptide sequence can be cut by the caspase 3 produced in the cell apoptosis process, thus indicating whether the cell enters an apoptosis state. Compared with the existing fluorescence enhancement apoptosis diagnosis kit, the preparation method disclosed by the invention is simple; the enzyme-sensitive fluorescence enhancement nano developer disclosed by the invention has favorable biocompatibility; the activity detection of a specific enzyme related to apoptosis can be completed in an in-vitro environment and a cell cracking solution through the detection of fluorescent signals; and the cell apoptosis state can be monitored on a living cell level.

The invention discloses a targeting gene-viro-therapy medicine specific for prostate cancer. An adenovirus is used, a natural promoter of an early gene EIA of the adenovirus is replaced by a promoter DD3 specific for the prostate cancer, and an oncolytic adenovirus is formed and carries anti-oncogene PTEN specific for the prostate cancer. If the anti-cancer effect of the anti-oncogene PTEN is not strong enough and is insufficient to completely kill the cancer, genes such as TRAIL, IL-24, MNSOD, CD, Smac, GM-CSF, IFN, IL-12, p53, RNAi, microRNA, Caspase 3 and Bax can added to the same carrier to be commonly used with the anti-oncogene PTEN, or two genes are linked to used through various schemes. The gene-viro-therapy medicine specific for the prostate cancer has high targeting treatment effect on the prostate cancer and basically has no influence on normal cells.

The invention discloses a specific gene-virus therapeutic drug for colorectal cancer. A natural promoter of an early gene E1A of an adenovirus is substituted by a colorectal cancer specific promoter CEA to form an oncolytic adenovirus carrying a specific antitumor gene ST13 of colorectal cancer. If the antitumor effect of the oncolytic adenovirus is not strong enough to kill all the cancer cells, the following genes may be added to a same vector with the oncolytic adenovirus for common usage: TRAIL, IL-24, MnSOD, CD, Smac, GM-CSF, IFN, IL-12, p53, RNAi, microRNA, Caspase 3 and Ba*; or two genes can be connected through various schemes. The gene-virus therapeutic drug for colorectal cancer provided by the invention has high therapeutic effect on targeting colorectal cancer, and has no effect on normal cells.

There is provided a hair tonic comprising at least two of an inhibitor against 5α reductase type 2, an inhibitor against transforming growth factor β2, and an inhibitor against caspase-3; a method comprising screening for at least two of inhibition against 5α reductase type 2, inhibition against transforming growth factor β2, and inhibition against caspase-3, or comprising screening for inhibition against caspase-3 and then for apoptosis inhibition, and a hair loss inhibitor having the effect of inhibiting caspase-3, and a hair loss inhibitor having the effect of inhibiting caspase-3 and of inhibiting apoptosis.

The invention discloses a tumor radio sensitization medicine which has an active component of berberine. Proved by research: the berberine has the following efficacy of: 1, breast cancer cells are treated by berberine, which can induce dose-dependently G0/G1 stage cell retardation and apoptosis; 2, the berberine remarkably reduces the expression level of cell cycle control associated protein cyclin B and apoptosis resisting protein Bcl-2 and increases the expression level of apoptins Bax and caspase-3; and 3, the breast cancer cells treated by the berberine remarkably improve the sensitiveness of the cells to radiotherapy. The tumor radio sensitization medicine can improve the treatment effect of tumor radiotherapy, lower the exposure dose of the radiotherapy of a tumor patient, and lower the toxic and side effects brought by the radiotherapy, thereby improving the living quality of patients.

The invention discloses application of rabdocetsin in preparing a product for inhibiting proliferation of esophageal squamous carcinoma cells. Proofed by experiment, the application has the advantages that the rabdocetsin can effectively inhibit the proliferation of the esophageal squamous carcinoma cells, the cloning formation of the esophageal squamous carcinoma cells, affecting the cycle progress of the esophageal squamous carcinoma cells, inducing the retardation of the cycle of the esophageal squamous carcinoma cells, inhibiting the DNA (deoxyribonucleic acid) restoration of the esophageal squamous carcinoma cells, inducing the withering of the esophageal squamous carcinoma cells, regulating up the expression amount of cleaved-caspase-9, regulating up the expression amount of cleaved-caspase-3, regulating up the expression amount of cleaved-PARP, inhibiting Akt signal pathways, inhibiting NF-kappa B signal pathways, and inhibiting the growth of tumors caused by the esophageal squamous carcinoma cells; the important application value is realized.

The invention is intended to develop a drug capable of directly or indirectly inhibiting the activation of caspase. Specifically, the invention provides a caspase 3 inhibitor comprising a protein comprising the same or substantially the same amino acid sequence as that represented by SEQ ID NO: 1, 2, 3 or 31 or a salt thereof. The protein of the invention, a partial peptide or a salt thereof is useful as a pharmaceutical such as a prophylactic and/or therapeutic agent for AIDS, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, pigmentary retinopathy, cerebellar degeneration, myelodysplastic syndrome, aplastic anemia, sideroblastic anemia, myocardial ischemia, conduction disturbance, chronic cardiac failure, graft-versus-host disease, or congenital or acquired enzymatic defect.

A method for preventing UV-induced skin-cellular injury by using a green algae extract and a cosmetic composition containing the green algae extract are disclosed. An effective dose of the green algae extract is used to protect fibroblasts from UV-induced apoptosis. The mechanism of the disclosed method is using the green algae extract to inhibit interaction between apoptosis pathway molecules Fas/FasL so as to inhibit an adapter protein (FADD) in a death-inducing signaling complex (DISC) and in turn to inhibit caspase-3 activation and cleaved polymerase (PARP) such that irreparable damage to DNA can be prevented. The green algae extract can be mixed with a skin permeable cosmetic composition so that the cosmetic composition possesses the function of preventing skin from UV-induced injury.